This article first appeared in Allergic Living magazine. Updated: Feb. 18, 2015

THE ANCIENT Egyptians were said to revere the cat, glorifying it in hieroglyphs, depictions of deities and artwork. While today’s domestic kitty may not enjoy the same royal treatment, the feline still wields serious power: just being in the same room as one can trigger itching, coughing, wheezing and even a full-on asthma attack in the millions who have cat allergy.

The American Academy of Allergy, Asthma and Immunology says the condition affects an estimated 50 million Americans, including the 30 percent of those with allergic asthma who list cat dander as a key trigger.

Other than simply avoiding cats, immunotherapy, or allergy shots, is the only current treatment option for this allergy. The idea here is to re-train the immune system to accept the cat’s allergy-inducing protein rather than react to it as a dangerous invader.

To do so, the doctor injects small amounts of cat protein extract into the body over several visits, slowly increasing the dosage and then staying at a target level for three to five years. The hope is to achieve desensitization, or at the very least, greatly reduced symptoms.

The process is far from ideal. Not only does it require close to 100 injections, it is incredibly time-consuming, with untold hours spent at the doctor’s office. Not surprisingly, many patients simply quit going. Immunotherapy also always carries a reasonable risk of reaction, since the very thing a person is allergic to is being injected into the body. Anaphylaxis to immunotherapy, while uncommon, certainly has been reported, which is why patients are meant to wait at least half an hour in the doctor’s office after receiving an injection.

This is all that’s available today. However, the big news in the allergy and asthma research community is that a new, quick, and seemingly effective treatment for cat allergy looms large on the horizon, holding the promise of an end to the widespread grief.

Reports from a recently completed clinical trial speak for themselves. After just four shots of the new product – named Cat-SPIRE – patients experienced a significant decrease in symptoms when exposed to cat allergens. Not four shots per month or year, but just four shots in total, each taken one month apart. Two years later, the results were largely the same.

“That took us all by surprise,” says Mark Larché, an immunologist and professor of medicine at McMaster University in Hamilton, Canada. “To get a two-year effect after just one course of treatment, particularly when it’s only four injections, that’s very encouraging.” Larché is the co-founder of Circassia Ltd., a British biotech firm that is spearheading the product’s development along with the Canadian company Adiga Life Sciences, which is jointly owned by Circassia and McMaster University.

The key to Cat-SPIRE is the science behind the shot. Circassia scientists take the allergenic cat protein, called Fel d1, and break it down into basic parts called peptides. The building blocks of proteins are called amino acids, and peptides are strings of two or more amino acids. The Fel d1 protein is normally 162 amino acids long, while Cat-SPIRE contains seven synthetic peptides, each 15 amino acids in length, and each hand-picked to generate the desired response.

“Currently available immunotherapy basically takes the thing you’re allergic to and injects it into you,” says Steve Harris, CEO of Circassia and director of Adiga Life Sciences. Cat-SPIRE, he explains, was created by zeroing in on parts of Fel d1 that promote a regulatory, or non-allergic, immune response. By using fragments of Fel d1 created in a lab as opposed to the entire protein, fewer shots are needed, reactivity is lessened, increases in dosage are not required, and so far, the results have been impressive.

Patients have now been recruited for a final (or phase 3) trial that will confirm the shot’s effectiveness and also test whether giving eight injections instead of four makes any difference. About 1,400 cat-allergic individuals between the ages of 12 and 65 have enrolled in the trial, which is taking place in multiple sites across the United States, Canada and Russia over the next year.

Yet researchers already know that the shot won’t be equally effective for everyone. Dr. Harold Nelson, the principal investigator of the phase 3 trial, is quick to point out that patients in the previous trial showed an average symptom reduction of 50 percent. This suggests that Cat-SPIRE probably has a strong effect for many individuals, while others will likely benefit to a lesser degree.

Adults and children who experience anaphylaxis do not always receive live-saving epinephrine, according to findings from a three-year Canadian study.

“In adults, our study indicates that almost 50 percent of severe reactions are not treated with epinephrine in or outside of the hospital,” says Dr. Moshe Ben-Shoshan, a pediatric allergist at Montreal Children’s Hospital and a key researcher behind the Cross-Canada Anaphylaxis Registry.

Started in 2011, the registry, known as C-CARE, has collected data from approximately 1,500 allergic adults and children who visited emergency departments in British Columbia, Ontario and Quebec hospitals. The goal was to gain insights into the triggers and management of anaphylaxis.

In a related research paper from the C-CARE data, the rates of epinephrine use in children having reactions proved to be better than the adult patients, but could still stand improvement. Data collected from the Montreal Children’s Hospital emergency department showed that the most common triggers for reactions were peanut and tree nuts, and that nearly 1 in 3 children experiencing reactions did not receive epinephrine. Almost all of these children had been prescribed auto-injectors.

The children not receiving epinephrine were given either antihistamines or corticosteroids to bring a reaction under control. “Antihistamines and steroids are not established as primary management of anaphylaxis and further,” Ben-Shoshan said in an interview. “The only drugs that stops the progression of anaphylaxis is epinephrine.”

Antihistamines and steroids may treat visible symptoms such as hives, they do not tackle the systemic symptoms such as cardiac or breathing issues. Therefore, the allergist says, not using epinephrine right away can actually make a person’s condition worse.

Ben-Shoshan cites the case of one allergic teenager who ate a cookie she was handed as a store sample. She quickly realized the cookies contained peanut butter, and her mouth began to itch. She did not have her epinephrine auto-injector with her, so a friend drove her to the emergency department. When she arrived, she was walking, talking and had only minor symptoms. Within a few minutes, she collapsed. She received CPR and an epinephrine drip to stabilize her condition, and was admitted to intensive care where she later recovered.

“Had she injected [epinephrine] promptly, all the studies indicate that she is not likely to have deteriorated the way she did,” says Ben-Shoshan. The C-CARE data found that the prompt use of epinephrine may also prevent the need for additional doses of the drug in the emergency department.

The low rate of epinephrine use among adults experiencing anaphylaxis is a growing concern. Ben-Shoshan suggests the trend likely relates to concern about side effects, a common misconception. (In fact, the C-CARE data reveals that most of the adults who used the drug experienced no side effects.) The researcher says that it’s also not uncommon for patients to make a “distorted link” between giving epinephrine and having to go to the hospital, believing that if they don’t administer epinephrine, the reaction is less severe and they can stay home.

“On the contrary, if you don’t give epinephrine, you’re more likely to deteriorate and end up at the hospital,” he says. The registry data also show that nearly half of the adult patients with moderate-to-severe reactions did not own a prescribed auto-injector.

C-CARE, funded in part by AllerGen, is the world’s first registry to track anaphylaxis occurrences as they are reported, and the researchers plan to publish the four-year findings in 2015.

The medical guidelines state that any serious allergic reaction requires epinephrine. “It’s clearly indicated. It’s the educational programs that need to be distributed and implemented,” says Ben-Shoshan.

A new study is shedding light on why women often have it worse when it comes to anaphylaxis.

It has long been observed that women experience allergic reactions that are more severe compared to men, but clinicians did not understand why – until now. Research recently published in the Journal of Allergy and Clinical Immunology pinpoints estrogen as the culprit.

The study, conducted by researchers from the National Institute of Allergy and Infectious Diseases, used mice to investigate the biology behind the difference between the sexes. Researchers noted that female mice had more severe, longer lasting anaphylactic reactions compared to their male counterparts – similar to trends observed in humans – however, by reducing the estrogen levels in female mice, this gender disparity disappeared.

“We showed that when you take out the ovaries – you ovariectomize the mice – then there is no difference between the reactions of ovarectimized mice and males,” explains study co-author Dr. Ana Olivera. However, when Olivera and her colleagues injected the ovary-less female mice with estradiol, a type of estrogen, they observed much bigger anaphylactic reactions, indicating “that estrogen is a player in the severity of the response.”

Upon closer examination, researchers discovered that estrogen increases the activity of the enzyme – endothelial nitric oxide synthase (eNOS) – that causes tissues to swell and blood vessels to widen, resulting in anaphylactic symptoms such as rashes, breathing issues, and in severe cases cardiac arrest.

So what does all of this mean for women with food allergies?

“It provides a rationale for doctors to perhaps use other treatments in cases of very strong anaphylactic reactions particularly in women,” says Olivera. According to the NIAID scientist, these treatments could include using medication to inhibit the eNOS enzyme in women who suffer from severe anaphylaxis or simply advising women to take extra precautions at times when their estrogen levels are high, such as right before menstruation or during puberty.

Olivera says with these findings she hopes to make people, particularly women, more aware of the factors involved in their reactions and help improve clinical management.

Medical research into finding a long-lasting food allergy treatment has just been given a huge shot in the arm. Billionaire tech mogul Sean Parker, the former president of Facebook, is donating $24 million to Dr. Kari Nadeau and her team at Stanford University.

The funds will be used to create the Sean N. Parker Center for Allergy Research, and to ramp up the scientific work of immunologist Nadeau and her team, as well as collaborators at other sites.

Parker and Nadeau have ambitious objectives. In a media conference call, they spoke of making “catalytic change” and moving toward a therapy that takes only one or two treatments, retrains the immune system at the cellular level – and lasts.

“The goal is really important to keep in mind,” said Parker. “It’s not just enough to come up with slightly better incremental improvements on the treatments that are out there, the goal is to achieve a cure.”

Parker, who famously started Napster before working with Mark Zuckerberg to make Facebook a global phenomenon, has a personal stake in seeking tech-style disruption in the world of allergy research. He’s at risk for anaphylaxis to several foods, including peanuts, other legumes, nuts and shellfish. He has needed emergency hospital care for both anaphylaxis and asthma – “my wife claims it’s been 14 times since we’ve been dating (they met in 2010) and now married. So it dramatically affects your life and, if you have a comorbidity such as asthma, it’s a much more severe problem.”

Dr. Kari Nadeau

As the father of two young children (his son was born in early December), Parker is also highly aware of the genetic component of allergies. Referencing the breathing issues he’s had with asthma and seasonal allergies, and the risks from trace amounts of food allergens, Parker notes: “It would be incredible if nobody, including my children, ever had to go through this.”

Nadeau is definitely among the researchers on the forefront of finding a successful treatment for food allergy. The field began to move ahead with oral immunotherapy or OIT in which miniscule, then gradually increasing amounts of an allergen are fed to an allergic person with the goal of desensitizing to a single allergen.

But that therapy has not been without sometimes serious side effects and setbacks, such as a 2013 Johns Hopkins University long-term follow-up study that found a majority of patients who were supposed to be desensitized still having symptoms – sometimes serious ones.

This does not deter Nadeau, since her work has already moved beyond OIT on its own. “Oral immunotherapy alone is helpful in many patients, but it doesn’t work in everyone,” she said on the media call. Much of her success at Stanford in the past three years has focused on the combination therapy of anti-IgE medication (known by the brand Xolair) followed by OIT to treat up to five food allergies at once.

It appears the immunologist and the new research center are planning to move forward with new clinical trials as early as 2015. Although Nadeau can’t yet be specific, in a press release she says she views Parker’s gift “as the springboard to improve the lives of those adults and children with allergies through immunotherapy that goes beyond oral therapy.”

On the media conference call, she and Parker both stressed an intriguing fact about food allergy. “We know that there are some people out there who had food allergies when they were children but naturally lost those allergies,” said Nadeau. “So we know that the immune system can be turned off. It can become non-allergic. The big question is ‘how’? How can we do it?”

Her team will be looking for key biomarkers in those who are sensitized, and in those who become desensitized. “I think it’s going to take combination therapies, I think we have to be smart about collaborating (with other centers) – we need to collaborate and share data,” she says.

Parker speaks of a fascination with the workings of the immune system, and has also given generously to immune-based cancer research. Aside from expressing confidence in Nadeau’s abilities as a researcher and immunologist, he is impressed by the level of patient involvement at Stanford – the clinic has a waiting list of 1,500 would-be desensitization patients. For clinical trials, he notes, “patient recruitment is almost as challenging as the science itself.”

So will he join the trials at the center that will soon bear his name? “There are some things on the horizon that are very promising, and I’ll be the first in line to try them,” Parker said. “I’m confident enough, that I’m probably going to be one of the first people to enter those trials when they open.”

The skin may hold the answer as to why some children develop peanut allergies before they’ve even eaten a single peanut, suggests new research.

Dr. Helen Brough is the lead author of a groundbreaking British study that reveals how exposure to peanut residue in household dust can increase the risk that children with eczema or other skin conditions will go on to develop peanut allergy.

Allergic Living has an exclusive interview with Dr. Brough but first, some background on the study:

Researchers vacuumed sofas in the homes of 577 U.K. babies in their first year of life.

Detectable peanut protein was found in more than 1/3 of the dust samples.

Years later, at ages 8 and 11, the children in this same study group were tested for peanut allergy, as well as mutations of the FLG skin gene (such mutated genes are strongly associated with eczema).

Of those who had become peanut-allergic, 1 in 5 had the mutated FLG gene.

In homes with 3 times as much peanut in the dust, a child with the mutated gene was 3 times more likely to develop peanut allergy.

“Previously it was thought that children developed a predisposition to becoming peanut allergic by exposure to peanut from maternal peanut consumption during pregnancy or breastfeeding,” explains Dr. Brough, an honorary senior lecturer at King’s College London. “This study suggests that there may be an alternative route by which children might develop become peanut allergic – and that is through exposure to peanut through the skin.”

In the following interview with Associate Editor Ishani Nath, pediatric allergist Dr. HelenBrough discusses her groundbreaking study and what it could mean for our understanding of how peanut allergies develop.

Allergic Living: What is it about the skin and its immune system that is leading to allergy?

Dr. HelenBrough: In children with porous skin (due to FLG mutations) allergens are thought to penetrate the skin and predispose the body towards an allergic response. There is evidence that disruption of the skin – through constant scratching, irritation or inflammation – leads to an allergic immune response in the skin. Peanut could therefore penetrate disrupted skin when the immune system is predisposed towards allergy, and lead to a peanut-allergic response.

Infants in the study who did not have the mutated FLG gene were safe from the effects of peanut proteins in household dust.

AL: How does peanut protein get into household dust?

DB: Peanut can be measured on hands and in saliva at least three hours after eating a peanut-containing meal. Thus, peanut can be transferred into the environment by hands or saliva, for example onto bedding while asleep, for some time after eating peanuts.

AL: If you don’t eat peanuts in your home, will there still be peanut protein in your household dust?

DB: In our study, peanut protein was found in the dust of the infant’s bed and play area in about 10 percent of homes where there was no or minimal household peanut consumption. This may have been due to other friends and family visiting the home who did eat peanut.

The new CEO of FARE is a man of science with a vision for the future that includes finally finding effective treatments for the 15 million Americans who live with food allergies and the risk of anaphylaxis.

Dr. James Baker equally sees the importance of continuing to escalate Food Allergy Research & Education’s role in building awareness. “Our overall priority is to educate and advocate for people with food allergies, and try to get the rest of the population to appreciate the difficulties these patients have and to make accommodations for them,” says the allergist, immunologist and former pharmaceutical executive who took the reins on Oct. 30, 2014 as both FARE’s new CEO and chief medical officer.

Baker had been working as FARE’s interim leader since the departure of the previous CEO, John Lehr, and was previously a member of the leading not-for-profit’s research advisory board. He brings the interesting combination of a background in pharmaceuticals and allergy and immunology research to his new position. He is a former senior executive at Merck, the former director of the Michigan Nanotechnology Institute, and Baker started the Food Allergy Research Center within the University of Michigan’s Division of Allergy and Clinical Immunology.

“We’ve been hamstrung to a great degree in allergy,” says the new CEO. “We can reduce the symptoms after an allergic attack has occurred, we can do things that try to reduce people’s sensitivity, but none of these are a cure.”

FARE funds significant research into oral immunotherapy (OIT) and other desensitization treatments, and Baker further sees a role for potential drug therapies in food allergy. “What I hope to do is bring my background, not just from basic science research but also from translational research and the pharmaceutical industry, so that we really develop the type of transforming drugs that will change the lives of people with food allergy,” he says.

He relates intriguing examples, such as the drug Dupilumab, which has been shown to be effective in blocking atopic dermatitis and asthma. He notes that “the fact that [the drug] knocks out both of these allergic diseases also raises the likelihood that it will be effective for food allergy as well.”

In his role on the research advisory board, the new CEO played an instrumental role in shaping FARE’s research strategic plan, called A Vision and Plan for Food Allergy Research. In the coming years, he hopes to encourage and provide the infrastructure necessary for new testing and studies through a network of research centers that FARE is developing.

Beyond research, Baker is eager to advance FARE’s role in food allergy education and advocacy. In the interview with Allergic Living, he highlighted three areas of focus:

Schools: The epidemic of food allergies presents a particular challenge to schools. Baker sees a role for FARE in ensuring that U.S. schools have the resources and capability to accommodate students with food allergies properly, and to be prepared in case of severe allergic reactions.

Restaurants: FARE plans to work with restaurateurs to broaden the safe dining options for those with food allergies, exploring options such as identifying allergy-friendly restaurants through websites and apps.

Adults with allergies: Later on in life, food allergies can create complications in terms of job availability and workplace environments. For instance, those with food allergies are unable to enlist because the military cannot at present customize food content. Baker sees FARE playing a role in helping people with food allergies at every stage in their lives.

The new CEO is in touch with the needs of those with food allergies. “I’ve taken care of patients with allergies, and specifically food allergies, for 35 years and I’ve seen the range of problems this creates. This really affects every facet of an individual’s life.”

His plans for improvement are not limited to these few bullet notes. “My hope is to strengthen FARE’s role as the leading organization working on food allergy in the U.S. We really need a voice across the country that communicates the issues that relate to food allergy patients and advocates for them both medically and legally.

“And I’d like to make sure that we continue to work for access and, very importantly, for appropriate care for patients with food allergy.”

From the Allergic Living archives. First published in the magazine in 2010.

AVOID, AVOID, avoid. That’s how Ann Jeannette Glauber had been treating her 4½-year-old son’s allergies to eggs, milk, peanuts, nuts and shellfish. But at a party a few years ago, Theo grabbed and ate a handful of Goldfish crackers (which contain dairy) before she could stop him.

“I kind of freaked out,” she admits, since her son had previously had an anaphylactic reaction to cottage cheese. Theo didn’t react to the crackers, but avoidance remained the family watchword.

The boy, however, turns out to be among the 75 per cent of kids allergic to dairy whom researchers now believe can actually tolerate milk – provided it has been extensively heated through baking. The same holds true for egg.

While under supervision at Johns Hopkins University School of Medicine in Baltimore, Theo on separate occasions was able to eat one-twelfth of an egg and a quarter cup of milk, both of which were baked into a cake. Emergency treatment was at the ready, but he didn’t react. By May, the boy had started a new diet at home that includes muffins, breads, even croissants; foods thoroughly baked at 350 degrees for at least 30 minutes. There has been a sanctioned bite of lasagna and, in the next phase, Theo will be testing out pizza, which isn’t cooked as long.

Allergists have long heard stories of allergic children who have accidentally eaten milk or egg – perhaps grandma fed the child an off-limits cupcake, or a daycare provider didn’t realize that cookies contained egg – without reactions.

But researchers are getting closer to understanding why kids like Theo can tolerate milk or egg that has been baked, while others still will react immediately. They’re also finding that introducing the baked food into the diet may actually help the child outgrow the allergy.

At Johns Hopkins, some dairy-allergic kids, including those who have had significant reactions to milk in the past, have even moved on to unheated foods such as yogurt and chocolate milk.

The best news: this is research that doesn’t have to wait for clinical trials and government approvals. As long as you begin at the office of your allergist, and he or she has the resources to perform food challenges safely, introducing baked milk or egg into your child’s diet is “something that can be done right now,” Dr. Wesley Burks, head of pediatric allergy and immunology at Duke University Medical Center, told the American Academy of Allergy, Asthma & Immunology conference in New Orleans earlier this year. He called this new way of treating milk and egg allergy a “paradigm change.”

Added Dr. Hugh Sampson, chief of allergy and immunology at New York’s Mount Sinai School of Medicine and leader of the research: “What it means is that as opposed to going to birthday parties and not being able to eat cake, or going to school and worrying about somebody eating a cookie that has milk or – they can suddenly do all this.”

***

THE CONCEPT of feeding allergic kids baked milk or egg goes against longstanding food allergy management practice and what parents like the Glaubers have been doing to protect their children. That is, they do everything in their power to ensure that not a morsel of the allergenic food crosses their child’s lips. A shift in thinking began a few years ago with a study performed by Sampson and his colleagues at Mount Sinai.

They gave each of 100 milk-allergic kids a muffin to eat that contained 1.3 grams of milk protein, in the form of dry milk powder. If a child was able to eat the muffin, baked for 30 minutes, without a reaction, two hours later he or she was served a waffle, which was only cooked for three minutes.

Sampson and his team found that 75 of the 100 children tolerated milk that had been extensively heated, and they were told to keep it in their diet.

While in the past it had been believed that kids were more likely to outgrow a milk allergy if they successfully avoided it, this study suggested otherwise. In follow-up appointments three months later, those children who had continued to eat baked milk products showed a significantly smaller

Peanut allergies are severe, often affecting children, and are increasing in prevalence. It’s no wonder researchers around the globe are looking at new, inventive ideas for how “cure” them, or at the very least, how to allow those with peanut allergies to tolerate at least a small amount of this legume’s protein.

Allergic Living looks at two of the latest ideas in the labs:

Peanut Allergy Vaccine

Researchers at Mount Sinai and Johns Hopkins University are studying a vaccine for peanut allergies to see if it is safe. The vaccine contains an altered peanut protein to “trick” the immune system. Dr. Scott Sicherer, an associate professor of pediatrics at the Mount Sinai School of Medicine in New York likens the changed peanut to a baby bracelet that spells “peanut.”

“If you altered that bracelet a little bit, let’s say you changed the ‘A’ in peanut to a ‘D’, then it would say PEDNUT instead of PEANUT,” he says.

The idea is that the person’s immune system won’t recognize “pednut” and won’t mount an allergic reaction to it. However over time, if it sees “pednut” enough, it may learn to tolerate “peanut.”

Once the safety trials for the vaccine, which is administered rectally as a suppository and also contains heat-killed E. coli, are complete, researchers will begin to study if it actually reduces peanut allergy in humans.

The Desensitizing ‘Peanut Patch’

Researchers are also looking at the possibility of desensitizing people with peanut allergies through the skin.

Dr. Hugh Sampson, head of the Consortium of Food Allergy Research in the United States, told Allergic Living magazine that U.S. researchers got the idea from French research, in which scientists have developed immunotherapy patches for cow’s milk allergy.

Those researchers placed a milk-containing patch on dairy-allergic patients every other day for three months. The results were that the patients were able to consume, on average, 12 times more milk without a reaction than they could before the treatment.

]]>http://allergicliving.com/2010/08/30/new-research-on-peanut-allergies/feed/0Toward a Cure for Celiac Diseasehttp://allergicliving.com/2010/08/27/toward-a-cure-for-celiac/
http://allergicliving.com/2010/08/27/toward-a-cure-for-celiac/#commentsFri, 27 Aug 2010 22:48:25 +0000http://allergicliving.ds566.alentus.com/?p=2607From a vaccine to a pill to a wheat sheaf without gluten, Allergic Living explores the exciting research treatment around the world.

Building Tolerance

Dr. Bob Anderson, a gastroenterologist in Melbourne, Australia, is heading the research on a celiac vaccine. His work focuses on desensitizing patients by injecting them with gluten peptides, amino acids that gang up to produce the immune reaction. “The idea is if you give one injection, you will activate a response but if you repeat it, you can use it as a treatment,” he tells Allergic Living.

Anderson has focused on a treatment that would allow people to eat gluten because he knows it’s hard to avoid the protein, no matter how diligent you are. He points to research that suggests about half of patients who are following gluten-free diets still have substantial damage in their small intestines. Results from the Phase I safety trial with patients should be compiled and ready by the middle of this year.

Gluten-free Wheat

The effort to change the very makeup of wheat is centred at Washington State University. Dr. Diter von Wettstein, a professor in the department of crop and soil sciences is trying to neutralize the parts of gluten that cause the immune reaction in the first place. The goals are to produce a celiac-friendly wheat that contains lysine, an essential amino acid often deficient in the grain, which would help to maintain the wheat’s baking texture and elasticity when it was made into dough.

“Creating new cultivars of wheat, arguably the most important crop grown … will be of tremendous benefit not only for sufferers of celiac disease, but for all consumers of wheat and wheat products,” von Wettstein said.

Popping a Pill

Research to develop a celiac “pill” includes trials taking place at Leiden University in The Netherlands, where Dr. Frits Koning and his team are testing a drug derived from a common fungus that can be found on decaying vegetation. Known as an AN-PEP, it is thought to break down both the gluten proteins and the T-cell peptides in the small intestine, preventing an adverse reaction. They’ve found the enzyme to be safe in humans, but haven’t yet proved its effectiveness.

In Baltimore, Dr. Alessio Fasano and his team have developed a pill that, rather than break down gluten, prevents gluten particles from penetrating the lining of the small intestine. Fasano says to imagine the small intestine as a gated community, with a protein called zonulin opening and closing the gates. In people with celiac disease, the gate is left ajar. A person would take the drug before eating, to block the release of zonulin. Phase III clinical trials for the pill are on hold, as the biotech firm that was to conduct them is struggling with funding. Fasano may partner with a larger firm. “One of the best assets of a scientist is perseverance. This drug could potentially be the next blockbuster. You have to have faith.”

First published in Allergic Living magazine.
To subscribe or order a single issue, click here.